Hemorrhagic Cystitis, Noninfectious 

  • Author: Joseph Basler, MD, PhD; Chief Editor: Edward David Kim, MD, FACS   more...
 
Updated: Sep 14, 2009
 

Background

Hemorrhagic cystitis is defined as an infectious or noninfectious process that leads to gross hematuria originating in the urinary bladder. Infectious causes of hemorrhagic cystitis include bacterial and viral etiologies. The various noninfectious causes are the topic of this discussion.

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Problem

Noninfectious hemorrhagic cystitis most commonly occurs in patients who have undergone pelvic radiation, chemotherapy, or both.[1] Affected patients may develop asymptomatic microscopic hematuria or gross hematuria with clots, leading to urinary retention. Treatment depends on the etiology, severity of the bleeding, and symptoms.[2]

Rarely, arteriovenous malformations, stones, metastatic tumors, and, more commonly, urothelial malignancies manifest as gross hematuria. These are differentiated from hemorrhagic cystitis with imaging and endoscopic evaluation.[3]

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Epidemiology

Frequency

Hemorrhagic cystitis occurs in up to 70% of patients exposed to high doses of cyclophosphamide or iphosphamide chemotherapy[4, 5, 6, 7] and up to 15% of patients who undergo pelvic irradiation to treat malignancy.[8, 9, 10] However, over the last several years, newer irradiation techniques have decreased the incidence of hemorrhagic cystitis to approximately 10% of treated patients.[11]

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Etiology

Noninfectious hemorrhagic cystitis is characterized by inflammation of the bladder associated with hematuria. Patients with this condition usually present with urgency, frequency, dysuria, and, in some cases, abdominal discomfort.

Although the causes of noninfectious hemorrhagic cystitis vary, this condition most commonly develops as a complication of pelvic radiation or from toxicity related to the use of certain chemotherapeutic drugs (eg, cyclophosphamide, iphosphamide). Less commonly, exposure to certain industrial chemicals, such as aniline or toluidine derivatives, causes hemorrhagic cystitis. Although rare, drugs such as penicillins or danazol can also precipitate hemorrhagic cystitis.

Other extremely rare reports include associations with food poisoning (Salmonella typhi)[12] and prolonged high-altitude air travel (Boon disease).[13] Regardless of the perceived circumstance, an infectious etiology should be sought as part of the initial assessment, even in the setting of radiation or chemical exposure, as infection may serve as an exacerbating factor. Bacterial, fungal, parasitic, and especially viral bladder infections in immunocompromised patients are often complicated by hemorrhagic cystitis.

Radiation-induced hemorrhagic cystitis

Nearly one fourth of patients who undergo pelvic radiation develop bladder-related complications. Slightly less than 50% of these patients develop diffuse hematuria. These patients have usually undergone radiation therapy for cancer of the prostate, colon, cervix, or bladder. Urgency, frequency, dysuria, and stranguria may develop acutely during radiation or may begin months to years after completion of radiotherapy. See the image below.

Irradiation cystitis changes after 7200 cGy externIrradiation cystitis changes after 7200 cGy external beam radiation for localized prostate cancer.

The symptoms of radiation cystitis are caused by a microscopic progressive obliterative endarteritis that leads to mucosal ischemia. The ischemic bladder mucosa then ulcerates and bleeding ensues. Neovascular ingrowth to the damaged area, as shown in the images below, then occurs, causing the characteristic vascular blush on cystoscopic evaluation. The new vessels are more fragile and may leak with bladder distension, minor trauma, or any mucosal irritation. Submucosal hemorrhage and overt hematuria may then begin precipitously. Acute episodes of radiation cystitis wane within 12-18 months in most patients following radiation therapy.[8, 9, 10]

Neovascularity associated with irradiation cystitiNeovascularity associated with irradiation cystitis. When distended, these weak-walled vessels often rupture, resulting in submucosal hemorrhage and gross hematuria. Bladder neck neovascularity after radiation therapBladder neck neovascularity after radiation therapy (IMRT) for prostate cancer.

As expected, the higher the dose and the wider the field encompassed by the radiation exposure, the more likely the sequelae of radiation cystitis. Patients who have undergone pelvic radiation are at an increased risk for radiation cystitis if additional radiotherapy is performed because of the cumulative dose effect. Infection, bladder outlet obstruction, and instrumentation are all factors that can exacerbate radiation cystitis.[14]

Drug-induced hemorrhagic cystitis

Chemotherapeutic drugs

The oxazaphosphorine-alkylating agents cyclophosphamide and ifosfamide are chemotherapeutic drugs that are useful in the treatment of lymphoma, leukemia, and certain solid tumors.[15, 16, 17]

Unfortunately, the toxicity of these drugs is not insignificant, and many of the adverse effects are urologic. Both microscopic and gross hematuria can result from the use of cyclophosphamide. The incidence of urologic adverse effects varies from 2%-40%, and the toxicity is dose-related. The onset of hematuria usually occurs within 48 hours of treatment.[18] Hemorrhagic cystitis due to ifosfamide therapy is generally worse than that caused by cyclophosphamide.[19] Cyclophosphamide is also associated with bladder cancer, typically aggressive.[20, 21]

Ifosfamide causes the release of tumor necrosis factor-alpha and interleukin-1 beta, mediating the release of nitric oxide and leading to hemorrhagic cystitis.[22, 23] Cyclophosphamide itself is not toxic; the drug's toxicity is due to its hepatic conversion to the metabolite acrolein, which is excreted in the urine and causes bladder edema and bladder hemorrhage. Over time, chronic bladder damage manifests as fibrosis with decreased capacity, trabeculations, and telangiectasias. The adverse effects of cyclophosphamide are more likely due to increased bladder exposure to acrolein.[24] Thus, patients receiving cyclophosphamide should always receive good hydration, and a Foley catheter is often placed to ensure immediate drainage of the bladder.[25] Continuous bladder irrigation is sometimes recommended to hasten acrolein clearance from the bladder.[26]

Penicillins

In rare cases, penicillins have been reported to cause hemorrhagic cystitis in certain patients. Case reports have implicated methicillin, carbenicillin, ticarcillin, piperacillin, and penicillin VK. Most cases of hemorrhagic cystitis in patients taking extended-spectrum penicillins have been reported in those with cystic fibrosis who had previously received penicillin antibiotics. Symptoms can take up to 2 weeks to develop after the drug is started; when symptoms occur, the best treatment is to discontinue the offending drug immediately. Hemorrhagic cystitis in patients taking penicillins is thought to be caused by an immune-mediated hypersensitivity. Examination of the urine frequently reveals eosinophils.[27, 28, 27, 29]

Danazol

Treatment with danazol, a semisynthetic anabolic steroid, has caused hemorrhagic cystitis in patients with hereditary angioedema. Interestingly, the advent of hemorrhagic cystitis in these patients followed years of symptom-free treatment with danazol. Hematuria developed after 30-77 months of treatment in one study. In almost all cases, the hematuria resolved after cessation of danazol. The dose of danazol did not correlate with the severity of hemorrhagic cystitis. The etiology of hemorrhagic cystitis in patients being treated with danazol is unclear.[30]

Other medications

Other medications that have been implicated in the development of hemorrhagic cystitis in limited reports include temozolomide,[31] bleomycin,[32] tiaprofenic acid,[33] allopurinol,[34] methaqualone,[35] methenamine mandelate,[36] gentian violate,[37, 38, 39, 40] , nonoxynol-9 suppositories inadvertently placed in the urethra,[41, 42] and intravesical acetic acid.[43] Risperidone has been associated with hemorrhagic cystitis but is also used as treatment for hemorrhagic cystitis due to JK virus.[44]

Other causes of noninfectious hemorrhagic cystitis

Environmental factors

Cases of hemorrhagic cystitis with no infectious etiology have been reported in patients whose occupation puts them in contact with certain urotoxic chemicals such as aniline (found in dyes, marking pens, and shoe polish) and toluidine (found in pesticides and shoe polish) derivatives. In these cases of hemorrhagic cystitis, the patient's exposure to the chemicals is usually work-related. Hemorrhagic cystitis due to these derivatives is self-limiting, and cessation of the exposure usually suffices for cure. Exposure to these chemicals also increases the risk of transitional cell carcinoma; thus, the workup for gross hematuria should reflect this possibility.[45]

Chlordimeform

The pesticide chlordimeform is commonly used on cotton plants and fruit trees, and ingestion, inhalation, or skin contact with this chemical can cause hemorrhagic cystitis. The toxicity of chlordimeform is likely due to one of its metabolites, 2-methylaniline, an aniline derivative. Hemorrhagic cystitis caused by chlordimeform is self-limiting, although whether these exposures increases the risk of bladder cancer is unknown.[46, 47]

Ether

Ether has been injected into the balloon ports of Foley catheters in an attempt to clear clogged ports and to deflate them, but this compound has an extremely toxic effect on the bladder. Balloons invariably rupture, and ether cystitis results in acute hematuria; long-term sequelae may include decreased capacity and irritative voiding symptoms.[48]

Vaginal products

A chemical hemorrhagic cystitis can develop when vaginal products are inadvertently placed in the urethra. Gentian violet douching to treat candidiasis has resulted in hemorrhagic cystitis when the drug was misplaced in the urethra, but this hemorrhagic cystitis resolved spontaneously with cessation of treatment.[37, 38, 39, 40] Accidental urethral placement of contraceptive suppositories has also caused hemorrhagic cystitis in several patients. The bladder irritation was thought to be caused by contact of the acidic compound nonoxynol-9 (pH, 3.35) with the bladder. In the acute setting, the bladder can be copiously irrigated with alkalinized normal saline to minimize bladder irritation.[41, 42]

Viral causes of cystitis

Although hemorrhagic cystitis associated with post solid-organ transplantation, bone marrow transplantation, or cord blood transplantation is not technically noninfectious, a short discussion is in order for completeness. Patients undergoing therapy to suppress the immune system are at risk for hemorrhagic cystitis due to either the direct effects of chemotherapy or activation of dormant viruses in the kidney, ureter, or bladder.[49, 50, 51, 52, 53, 54, 55, 56, 57, 58]

In the early 1990s, infection with polyomavirus or adenoviruses was implicated as the likely etiology of this condition. Polyomavirus is highly prevalent in the pediatric population and is thought to remain dormant and asymptomatic in the kidney and other organs after the initial infection. When the immune system is compromised, as in persons with HIV infection and those undergoing chemotherapy or chemical immunosuppression, the virus can be reactivated, leading to clinical nephritis, ureteritis, or cystitis.[59, 60]

The BK polyomavirus[61, 62, 63, 64, 65, 66, 67, 68, 69] and adenovirus types 7, 11, 34, and 35[70, 71, 72, 73, 74, 75, 76, 77, 78] have been the most commonly described viruses in these cases. Cytomegalovirus,[79, 80] JC virus,[81] and herpesviruses[38, 82, 83] have also been identified as causative agents in these scenarios.

HIV itself does not cause hemorrhagic cystitis but can predispose to other viral infections, such as BK virus, leading to the condition.[84] BK virus has also been shown to be a causal transforming agent for bladder cancer.[85]

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Pathophysiology

See Etiology.

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Presentation

Patients who present with hemorrhagic cystitis usually have a history of radiation or chemical exposure, and they are often inpatients or well known to their respective services.

The presence or absence of clotted blood is not completely helpful in determining the etiology of hemorrhagic cystitis, but the presence of long stringy clots suggests an upper–urinary tract etiology. Symptoms include suprapubic discomfort, urinary frequency, and inability to empty the bladder due to the clots.

Upon examination, the patient often demonstrates suprapubic fullness and discomfort or pain to palpation, as well as costovertebral angle tenderness if the bladder obstruction is chronic.

Differential diagnoses

The differential diagnoses of hemorrhagic cystitis include the following:

  • Active hemorrhage due to malignancy of the bladder, ureter, or kidney
  • Acute effects of urinary tract infection
  • Arteriovenous malformation
  • Calculi at any point in the urinary system

In males, prostatic varices may also be an underlying etiology of gross hematuria.

A history of trauma or recent manipulation of the urinary system (eg, catheterization, cystoscopy) suggests another etiology.

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Indications

Surgical intervention other than cystoscopy with cauterization is reserved for cases in which medical management fails. In extreme cases, when all other treatment options have failed, selective or superselective hypogastric branch artery embolization can be considered (see Surgical therapy).

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Relevant Anatomy

The bladder anatomy relevant to noninfectious hemorrhagic cystitis includes an appreciation of the layers from the lumen outward. The glycosaminoglycan (GAG) layer coats the inner surface over the transitional epithelium. Deep to this transitional epithelium, the bladder submucosa with its microvasculature overlies the detrusor muscle. A layer of fatty connective tissue surrounds most of the anterior and lateral bladder in the space of Retzius, while, posteriorly, the peritoneal serosal surface separates it from the cul-de-sac and abdominal cavity contents. In cases of chronic cystitis, neovascularity in the submucosal area is common and is presumably the site of acute hemorrhage. Ischemic changes of endarteritis can lead to mucosal ulcerations and acute hemorrhage.

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Contributor Information and Disclosures
Author

Joseph Basler, MD, PhD  Professor, Department of Urology, University of Texas Health Science Center at San Antonio; Chief, Section of Urology, Audie Murphy Veterans Affairs Hospital

Joseph Basler, MD, PhD is a member of the following medical societies: American Urological Association, Society for Basic Urologic Research, Society of University Urologists, Society of Urologic Oncology, Southwest Oncology Group, and Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Ryan Keith Miyamoto, MD  Staff Physician, Department of Urology, University of Texas Health Science Center, San Antonio

Ryan Keith Miyamoto, MD, is a member of the following medical societies: American Medical Association and American Urological Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Bradley Fields Schwartz, DO, FACS  Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine

Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Association of Military Osteopathic Physicians and Surgeons, Endourological Society, Society of Laparoendoscopic Surgeons, and Society of University Urologists

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Mark Jeffrey Noble, MD  Consulting Staff, Urologic Institute, Cleveland Clinic Foundation

Mark Jeffrey Noble, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Kansas Medical Society, Sigma Xi, Society of University Urologists, and Southwest Oncology Group

Disclosure: Nothing to disclose.

J Stuart Wolf Jr, MD, FACS  David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan

J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology

Disclosure: Terumo Corporation Consulting fee Consulting; Gyrus-ACMI Honoraria Speaking and teaching

Chief Editor

Edward David Kim, MD, FACS  Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center

Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, and Tennessee Medical Association

Disclosure: Lilly Consulting fee Consulting; Astellas Consulting fee Speaking and teaching; Indevus Consulting fee Speaking and teaching

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